Jun Zhu, Takanobu Taniguchi, Takashi Tanaka, Fumiko Suzuki and Ikunobu
Muramatsu*
Department of Pharmacology, School of Medicine, Fukui Medical University,
Matsuoka, Fukui 910-1193, Japan
*To whom correspondence should be addressed.
Abstract: In this study, [3H]hemicholinium-3 ([3H]HC-3)
binding, which labels the presynaptic high affinity-choline transport sites,
was examined in two brain regions, cerebral cortex and midbrain, of nicotine-treated
and -untreated rat neonates. In nicotine-untreated neonates, [3H]HC-3
binding sites of cerebral cortex increased from 64Êfmol/mg protein at postnatal
day 7 to 142Êfmol/mg protein at postnatal day 35. In nicotine-treated neonates,
the development of [3H]HC-3 binding sites in cerebral cortex
was significantly retarded, compared with control neonates on the 7th, 14th
and 21st postnatal days. In parallel with this, the development of muscarinic
receptor in cerebral cortex, which was detected by [3H]quinuclidinyl
benzylate ([3H]QNB) binding, was also retarded by nicotine treatment.
However, in midbrain, neither [3H]HC-3 nor [3H]QNB
binding sites at postnatal dayÊ14 was affected by nicotine treatment. These
results strongly suggest that perinatal treatment with nicotine inhibits
presynaptic and postsynaptic development of the cholinergic pathway in cerebral
cortex but not in midbrain of rat neonate.
Keywords: Nicotine, Development, Rat neonate brain,
[3H]Hemicholinium-3 binding (high affinity-choline transporter),
Muscarinic receptor
Copyright© The Japanese Pharmacological Society 2000
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